目的 探究阿魏酸在減輕大鼠腦梗死過程中對葡萄糖轉(zhuǎn)運蛋白（GLUTs）和神經(jīng)元葡萄糖代謝的影響。方法 72只SD大鼠隨機分為假手術(shù)組、模型組、尼莫地平組以及阿魏酸25、50、100 mg/kg組。采用Longa線栓法構(gòu)建腦梗死模型，梗死期間，模型組尾iv生理鹽水，阿魏酸組分別尾iv 25、50、100 mg/kg的阿魏酸治療，尼莫地平組尾iv 20 mg/kg尼莫地平，給藥3 d。完成給藥后24 h，對各組大鼠開展神經(jīng)功能評分，完成后取大鼠血液檢測外周血糖值，再通過PET/CT實驗檢測缺血區(qū)葡萄糖攝取水平。將大鼠處死后全腦組織進行TTC染色，取缺血核心區(qū)組織，通過比色法檢測ATP含量，采用Western blotting法檢測GLUT蛋白表達水平。結(jié)果 與假手術(shù)組比較，模型組大鼠神經(jīng)功能評分增加，出現(xiàn)明顯梗死區(qū)域，缺血核心區(qū)葡萄糖攝取量減少，ATP含量降低，GLUT1、GLUT3、PFKFB3蛋白表達降低（P＜0.05）。與模型組比較，阿魏酸50、100 mg/kg組大鼠神經(jīng)功能評分減少，梗死區(qū)域面積占比減少，缺血核心區(qū)葡萄糖攝取量增加，ATP含量升高，GLUT1、GLUT3、PFKFB3蛋白表達升高（P＜0.05）。結(jié)論 阿魏酸對腦梗死大鼠的治療效果與尼莫地平相似，其機制可能與提高GLUT1和GLUT3蛋白表達，促進葡萄糖向中樞神經(jīng)元轉(zhuǎn)運，提高葡萄糖代謝相關(guān)。

Objective To explore the effects of ferulic acid on glucose metabolism and GLUTamic acid in rats with cerebral infarction. Methods 72 SD rats were randomly divided into sham operation group, model group, nimodipine group, ferulic acid 25, 50, 100 mg/kg group. The cerebral infarction model was constructed by Longa line embolus method. During the infarction, the model group was treated with tail iv normal saline, ferulic acid group with tail iv of 25, 50, and 100 mg/kg respectively, and the nimodipine group with tail iv of 20 mg/kg nimodipine, the drug was administered for 3 d. 24 h after the administration of the drug, the rats in each group were collected to carry out neurological function scores. After the completion of the treatment, the blood of the rats was collected to detect peripheral blood sugar value, and then the glucose uptake level in the ischemic area was detected by PET/CT experiment. After the rats were killed, the whole brain tissues were stained with TTC, the ischemic core tissues were taken, ATP content was detected by colorimetry, and GLUTprotein expression level was detected by Western blotting experiment. Results Compared with the sham operation group, the neurological function score of the model group was increased, the infarction area was obvious, the glucose intake in the ischemic core area was decreased, and the ATP content was decreased (P < 0.05). The expression levels of GLUT1, GLUT3, and PFKFB3 protein were decreased (P < 0.05). Compared with the model group, the neurological function score was decreased, the percentage of infarction area was decreased, the glucose intake in the ischemic core area was increased, and the ATP content was increased in the ferulate acid 50 and 100 mg/kg group (P < 0.05). The expression of GLUT1, GLUT3, and PFKFB3 protein were increased (P < 0.05). Conclusions The therapeutic effect of ferulic acid on ischemic stroke rats is similar to nimodipine, and its mechanism may be related to increasing the expression of GLUT1 and GLUT3 protein, promoting the transport of glucose to central neurons, and improving glucose metabolism.

R966

自貢市重點科技計劃（2022ZCNKY22）